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This report is written by MaltSci based on the latest literature and research findings

What are the mechanisms of viral immune evasion? ​

Abstract ​

The ability of viruses to evade the host immune system is a critical factor in their pathogenicity and persistence, posing significant challenges for understanding viral biology and developing effective vaccines and antiviral therapies. This review explores the sophisticated mechanisms employed by viruses to escape detection and destruction by the immune system, categorized into innate and adaptive immune evasion strategies. Key tactics include alterations in viral antigens to prevent antibody recognition, inhibition of interferon signaling pathways, and disruption of antigen presentation mechanisms that thwart T cell responses. Notable case studies, including HIV, Influenza, and SARS-CoV-2, illustrate the diverse strategies of immune evasion. For instance, HIV's rapid mutation rate allows it to escape T cell recognition, while Influenza employs the non-structural protein 1 (NS1) to inhibit type I interferon signaling. SARS-CoV-2 downregulates MHC-I expression and induces hyper-inflammatory responses, complicating immune recognition. The insights gained from understanding these mechanisms are essential for informing vaccine development strategies and guiding the design of novel antiviral therapies. As viral infections continue to pose significant public health threats, particularly in the wake of emerging viruses, ongoing research is crucial to enhance host defenses and combat viral infections effectively.

Outline ​

This report will discuss the following questions.

  • 1 Introduction
  • 2 Mechanisms of Viral Immune Evasion
    • 2.1 Alteration of Viral Antigens
    • 2.2 Inhibition of Interferon Signaling
    • 2.3 Disruption of Antigen Presentation
    • 2.4 Modulation of Apoptotic Pathways
  • 3 Innate Immune Evasion Strategies
    • 3.1 Evading Pattern Recognition Receptors
    • 3.2 Counteracting Complement Activation
  • 4 Adaptive Immune Evasion Strategies
    • 4.1 T Cell Evasion Mechanisms
    • 4.2 B Cell Response Modulation
  • 5 Case Studies of Viral Immune Evasion
    • 5.1 HIV
    • 5.2 Influenza Virus
    • 5.3 SARS-CoV-2
  • 6 Implications for Vaccine Development
  • 7 Conclusion

1 Introduction ​

The ability of viruses to evade the host immune system is a crucial factor in their pathogenicity and persistence. This phenomenon, known as viral immune evasion, represents a significant challenge for both our understanding of viral biology and the development of effective vaccines and antiviral therapies. Viruses have evolved a myriad of sophisticated strategies to escape detection and destruction by the immune system, employing mechanisms that disrupt innate and adaptive immune responses. Understanding these mechanisms is not only vital for elucidating the dynamics of viral infections but also for designing innovative therapeutic interventions that can enhance host defenses.

Research in the field has demonstrated that viruses utilize various tactics to avoid immune recognition. These include alterations in viral antigens, inhibition of immune signaling pathways, and manipulation of host cellular responses [1][2]. For instance, some viruses can change their surface proteins to prevent recognition by antibodies, while others interfere with the interferon signaling pathways that are critical for mounting an antiviral response [1][3]. Additionally, viruses can disrupt antigen presentation mechanisms, thereby preventing T cells from recognizing and eliminating infected cells [1][4].

The significance of studying viral immune evasion mechanisms cannot be overstated. As viral infections continue to pose significant public health threats, particularly in the wake of emerging viruses such as SARS-CoV-2, a deeper understanding of how these pathogens manipulate host defenses is essential [2]. The insights gained from such studies can inform vaccine development strategies and guide the design of novel antiviral therapies that target specific evasion mechanisms [1][5].

Current research has identified several key mechanisms through which viruses evade the immune system. These mechanisms can be categorized into innate and adaptive immune evasion strategies. Innate immune evasion includes tactics such as evading pattern recognition receptors and counteracting complement activation [6][7]. Adaptive immune evasion, on the other hand, encompasses strategies that target T cell and B cell responses, effectively subverting the host's acquired immunity [8][9].

This review is organized as follows: we will first explore the various mechanisms of viral immune evasion, detailing how viruses alter their antigens, inhibit interferon signaling, disrupt antigen presentation, and modulate apoptotic pathways. Next, we will examine specific strategies employed by viruses to evade innate immunity, including the evasion of pattern recognition receptors and the counteraction of complement activation. Following this, we will discuss adaptive immune evasion strategies, focusing on T cell evasion mechanisms and the modulation of B cell responses. We will then present case studies of notable viruses, including HIV, Influenza, and SARS-CoV-2, to illustrate the diverse strategies of immune evasion in action. Finally, we will discuss the implications of these findings for vaccine development and therapeutic interventions, emphasizing the need for ongoing research to combat viral infections effectively.

In summary, understanding the mechanisms of viral immune evasion is critical for advancing our knowledge of viral pathogenesis and for developing effective strategies to enhance host immunity. The complex interplay between viruses and the immune system underscores the necessity for continued research in this vital area of biomedical science.

2 Mechanisms of Viral Immune Evasion ​

2.1 Alteration of Viral Antigens ​

Viral immune evasion is a sophisticated and multifaceted process that allows viruses to persist in the host despite the immune system's efforts to eliminate them. One of the primary mechanisms employed by viruses to evade immune detection is the alteration of viral antigens, which can significantly affect the host's immune response.

Viruses exhibit remarkable plasticity in their surface proteins, which are crucial for their recognition by the immune system. For instance, influenza viruses are known for their ability to escape the human antibody response by altering the amino acids in their surface proteins, particularly in hypervariable domains. This structural plasticity allows the virus to continuously change its antigenic profile, making it difficult for the immune system to recognize and mount an effective response against previously encountered strains (Crow 2012) [10].

Similarly, SARS-CoV-2, the virus responsible for COVID-19, has developed strategies to evade antibody neutralization through mutations in its spike protein. These mutations not only enhance the virus's ability to infect cells but also impair the immune system's ability to recognize and neutralize the virus. Specifically, SARS-CoV-2 proteins, such as ORF 6 and ORF 8, have been shown to downregulate MHC-I molecule expression, thereby reducing the effectiveness of cytotoxic T-cell responses (Rubio-Casillas et al. 2022) [2].

In addition to direct alterations of viral antigens, viruses can also manipulate host immune responses through various means. For example, they can interfere with antigen processing and presentation pathways, thereby preventing the effective recognition of infected cells by T cells. This interference often involves the modulation of host cytokine networks, which can create an immunosuppressive environment that further facilitates viral persistence (Eslami et al. 2025) [11].

Moreover, some viruses exploit mechanisms such as exosome-mediated communication to enhance their survival. By incorporating viral components into exosomes, viruses can cloak their antigens, effectively decoying the immune system and increasing their chances of evading detection (Anderson et al. 2016) [12].

The continuous evolution of viral antigens through mechanisms such as antigenic variation, as well as the strategic manipulation of host immune pathways, underscores the complex interplay between viruses and the immune system. Understanding these mechanisms is critical for developing effective antiviral therapies and vaccines that can counteract the sophisticated strategies employed by viruses to evade immune surveillance.

2.2 Inhibition of Interferon Signaling ​

Viral immune evasion is a critical factor in the ability of viruses to establish and maintain infection within a host. One of the primary strategies employed by viruses to achieve this is the inhibition of interferon (IFN) signaling, which is a crucial component of the host's antiviral response. The mechanisms by which viruses inhibit IFN signaling are diverse and sophisticated, allowing them to effectively counteract the host's immune defenses.

Firstly, viruses can prevent the initial detection of viral components by the host's immune system. This is achieved through the disruption of pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and retinoic acid-inducible gene I (RIG-I)-like receptors. By hindering the recognition of viral RNA or DNA, viruses can evade the triggering of the IFN response that would normally occur upon infection (Taylor & Mossman, 2013) [13].

Secondly, some viruses actively inhibit the production of type I IFNs. This can occur through the degradation or disarming of transcription factors essential for IFN gene expression, such as interferon regulatory factors (IRFs) and nuclear factor-κB (NF-κB). For instance, certain viral proteins have been shown to interfere with the phosphorylation and nuclear accumulation of IRF-7, which is critical for the induction of IFN (Zhu et al., 2002) [14]. Moreover, viruses can induce a general block on host cell transcription, thereby preventing the production of IFNs altogether (Schulz & Mossman, 2016) [15].

Additionally, once IFNs are produced, viruses can interfere with the signaling pathways activated by these cytokines. This is often accomplished by targeting the type I IFN receptor and disrupting the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway. By impeding this signaling cascade, viruses can inhibit the downstream effects of IFNs, including the activation of IFN-stimulated genes (ISGs) that play a vital role in establishing an antiviral state (Wang et al., 2018) [16].

Viruses also utilize more complex mechanisms to evade the IFN response. For example, they can co-opt cellular negative regulatory systems to their advantage, effectively using host pathways to inhibit the immune response. Some viruses produce proteins that bind to and sequester key components of the IFN signaling pathway, rendering them inactive (Devasthanam, 2014) [17].

Finally, recent studies have highlighted the role of viral non-structural proteins in suppressing IFN production. These proteins can inhibit the signaling pathways that lead to IFN production and block the expression of ISGs, further enhancing viral replication and persistence within the host (Chiang & Liu, 2018) [18].

In summary, the mechanisms of viral immune evasion, particularly through the inhibition of interferon signaling, involve a multifaceted approach. Viruses employ strategies to prevent detection by PRRs, inhibit IFN production and signaling, and utilize host regulatory pathways to subvert the immune response. Understanding these mechanisms is crucial for the development of effective antiviral therapies and vaccines.

2.3 Disruption of Antigen Presentation ​

Viral immune evasion is a critical aspect of viral pathogenesis, enabling viruses to persist within the host and evade immune surveillance. One of the primary mechanisms employed by viruses to achieve this is the disruption of antigen presentation, particularly through the inhibition of the major histocompatibility complex class I (MHC-I) pathway. This disruption has profound implications for the host's ability to mount an effective immune response.

Viruses utilize various strategies to interfere with the MHC-I antigen presentation pathway. For instance, certain viral proteins have been shown to downregulate the expression of MHC-I molecules on the surface of infected cells. This is exemplified by SARS-CoV-2, where the open reading frames (ORF) 6 and 8 produce viral proteins that specifically target and reduce MHC-I expression, thereby preventing the presentation of viral peptides to CD8+ cytotoxic T lymphocytes (CTLs) (Rubio-Casillas et al. 2022) [2]. Similarly, chronic viral infections such as those caused by HIV, HBV, and HCV also involve the downregulation of MHC-I molecules, disrupting the host's ability to recognize and eliminate infected cells (Eslami et al. 2025) [11].

Moreover, viruses may employ additional tactics to interfere with the intracellular processing of antigens. For example, some viral proteins can inhibit the transport of peptides to the endoplasmic reticulum, where MHC-I molecules are loaded with antigenic peptides. This interference limits the availability of peptides that would normally be presented to CTLs, thereby diminishing the immune response (Hansen & Bouvier 2009) [19].

The consequences of such disruptions are significant. By preventing the effective presentation of viral antigens, viruses can remain "invisible" to the immune system, particularly during the latency phase of infection. This is particularly evident in certain herpesviruses, where intrinsic, genome-encoded elements actively interfere with antigen processing and display (Wan et al. 2025) [20]. These mechanisms of primary sequence intrinsic immune evasion (PSI) not only limit antigen production but also contribute to the persistence of the virus in the host.

In summary, the disruption of antigen presentation is a multifaceted strategy employed by viruses to evade immune detection. By downregulating MHC-I molecules and interfering with antigen processing and presentation, viruses can effectively evade cytotoxic T-cell responses, thereby facilitating persistent infections and complicating vaccine development and antiviral strategies. Understanding these mechanisms is essential for the design of effective therapeutic interventions aimed at enhancing immune recognition and clearance of viral infections.

2.4 Modulation of Apoptotic Pathways ​

Viruses have evolved a variety of mechanisms to evade the host immune system, and one critical strategy involves the modulation of apoptotic pathways. Apoptosis, or programmed cell death, serves as a primary defense mechanism against viral infections, enabling the elimination of infected cells. However, many viruses have developed sophisticated tactics to manipulate these pathways to their advantage, thereby enhancing their survival and replication.

One of the fundamental mechanisms by which viruses evade apoptosis is through the direct inhibition of apoptotic signaling pathways. This includes the encoding of viral proteins that either inhibit pro-apoptotic factors or activate anti-apoptotic pathways. For instance, some viruses produce proteins that are homologous to host-derived apoptosis-regulatory proteins, such as members of the Bcl-2 family, which are known to inhibit the apoptotic process [21]. By mimicking these host proteins, viruses can effectively block the apoptotic signals that would typically lead to cell death.

Additionally, viruses can modulate the host's apoptotic machinery by interacting with cell surface receptors or components of the apoptotic pathways. For example, Human Immunodeficiency Virus (HIV) has been shown to alter normal apoptotic signaling, resulting in increased viral load and the establishment of viral reservoirs, which ultimately enhances infectivity [22]. The interactions of viral proteins with the host's pro- and anti-apoptotic responses play a crucial role in this dynamic, allowing the virus to manipulate the host cell environment to favor its own replication.

Furthermore, certain viruses may exploit the apoptotic machinery to eliminate uninfected immune cells, thereby reducing the overall immune response against the infection. This is particularly evident in the case of HIV, which activates apoptotic programs that destroy immune effectors, contributing to the chronic immune activation observed in infected individuals [23]. By doing so, HIV not only protects itself from the immune attack but also creates a more favorable environment for its propagation.

Moreover, the suppression of apoptosis is not limited to RNA viruses like HIV; DNA viruses, such as α-herpesviruses, have also developed multifaceted strategies to inhibit programmed cell death. These viruses encode anti-apoptotic factors that interfere with both the death receptor pathway and the mitochondria-mediated pathway of apoptosis, promoting their own replication and evasion of host defenses [24].

In summary, the mechanisms of viral immune evasion through the modulation of apoptotic pathways include the direct inhibition of apoptotic signals, manipulation of host cell responses, and the strategic activation of apoptosis in immune cells to diminish the host's defense. These tactics not only facilitate viral survival and replication but also highlight the complex interplay between viruses and the host immune system in the context of infection [21][22][25].

3 Innate Immune Evasion Strategies ​

3.1 Evading Pattern Recognition Receptors ​

Viral immune evasion is a critical aspect of viral pathogenesis, particularly in the context of the innate immune system, which serves as the first line of defense against viral infections. A central component of this system is the pattern recognition receptors (PRRs), which detect viral components and initiate antiviral responses. Viruses have evolved various strategies to evade detection by these receptors, thereby facilitating their replication and persistence within the host.

One prominent mechanism employed by viruses to evade PRRs involves the modification or sequestration of viral nucleic acids. For instance, viruses may alter their RNA or DNA to prevent recognition by intracellular sensors such as RIG-I-like receptors (RLRs) and cyclic GMP-AMP synthase (cGAS). This alteration can include the addition of caps or other modifications that inhibit the binding of PRRs, effectively masking the viral genome from immune detection [26].

Another strategy involves the interference with the signaling pathways activated by PRRs. Many viruses disrupt key signaling cascades, such as the nuclear factor kappa-B (NF-κB) pathway and the Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathway, which are crucial for the induction of type I interferons (IFNs) and other pro-inflammatory cytokines. For example, enteroviruses utilize specific proteases, such as 2A and 3C proteases, to cleave host proteins that are integral to immune signaling, thereby inhibiting the host's antiviral response [27].

Moreover, some viruses can directly target PRRs themselves, leading to their degradation or functional inhibition. This includes the cleavage of PRRs or their adaptor proteins, which prevents the downstream signaling necessary for an effective immune response [28]. For instance, the human immunodeficiency virus (HIV-1) has been shown to exploit host proteins to evade DNA sensing mechanisms, particularly through the action of TREX1, a host exonuclease that plays a role in the recognition of viral DNA [28].

In addition to direct targeting, viruses can also manipulate the cellular environment to create conditions that are unfavorable for PRR activation. This includes the sequestration or relocalization of PRRs away from their sites of action, thus preventing them from engaging with viral components [29]. The ability of viruses to modulate these pathways underscores their evolutionary adaptation to circumvent host defenses.

The complexity of viral immune evasion mechanisms illustrates a dynamic interplay between viruses and the host immune system. Understanding these mechanisms at a molecular level is crucial for developing effective vaccines and antiviral therapies, as it can provide insights into potential targets for intervention [30].

In summary, viral evasion of innate immunity, particularly through the evasion of PRRs, involves a multifaceted approach that includes modification of viral nucleic acids, disruption of immune signaling pathways, direct targeting of PRRs, and manipulation of the host cellular environment. These strategies collectively enhance viral replication and persistence, posing significant challenges for the host immune response.

3.2 Counteracting Complement Activation ​

Viruses have evolved a range of sophisticated mechanisms to evade the host's immune responses, particularly targeting the complement system, which is a crucial component of innate immunity. The complement system operates through three primary pathways: the classical, alternative, and lectin pathways, leading to the opsonization of pathogens, inflammation, and cell lysis. The ability of viruses to counteract complement activation is essential for their survival and propagation within the host.

One significant strategy employed by various viruses is the inhibition of complement activation. For instance, many viruses produce proteins that can directly interfere with complement components, thereby preventing the formation of the C3 convertase, which is critical for downstream complement activation. This strategy is vital as complement activation not only leads to the opsonization of viral particles but also triggers inflammatory responses that can eliminate the virus.

Moreover, viruses have been shown to exploit complement regulatory mechanisms to their advantage. They can mimic host proteins or utilize viral proteins that resemble complement regulators to inhibit complement activation. For example, the complement evasion strategies discussed by Favoreel et al. (2003) highlight how certain viruses can block complement activation pathways, thus avoiding recognition and clearance by the immune system[31].

Another mechanism involves the use of the complement system to enhance viral infectivity. Some viruses can bind to complement components or receptors, which may facilitate their entry into host cells or help them establish a latent infection. This interaction not only aids in evading the immune response but can also manipulate the immune system to create an environment conducive to viral replication and persistence[32].

Additionally, specific viruses have developed mechanisms to modulate the inflammatory responses triggered by complement activation. By doing so, they can reduce the effectiveness of the immune response while simultaneously promoting their own replication and spread. This manipulation of the host's immune response is a common theme among many viral pathogens, including those causing significant diseases[33].

In summary, the mechanisms of viral immune evasion through counteracting complement activation are multifaceted. They include direct inhibition of complement components, exploitation of complement regulatory proteins, and manipulation of the inflammatory responses associated with complement activation. Understanding these strategies is crucial for developing effective vaccines and therapeutic interventions against viral infections[34][35].

4 Adaptive Immune Evasion Strategies ​

4.1 T Cell Evasion Mechanisms ​

Viral immune evasion represents a significant challenge in the context of adaptive immunity, particularly concerning T cell responses. The mechanisms through which viruses evade T cell immunity are diverse and complex, often involving sophisticated strategies to undermine the host's immune recognition and response capabilities.

One primary mechanism of T cell evasion is the alteration of viral epitopes. Viruses can accumulate mutations in T cell epitopes, which leads to the loss of recognition by virus-specific CD8+ T cells. This phenomenon has been well-documented in the context of HIV-1, where the virus employs non-synonymous mutations to escape detection by the immune system, resulting in a significant loss of T cell recognition and a consequent failure to control the infection [36].

Another notable strategy is the manipulation of the major histocompatibility complex (MHC) class I antigen presentation pathway. Many viruses have evolved proteins that interfere with the presentation of viral peptides on MHC class I molecules, thereby preventing CD8+ T cells from recognizing and eliminating infected cells. This form of immune evasion has been extensively studied in herpesviruses, which utilize various mechanisms to disrupt the normal processing and presentation of antigens [37].

Additionally, T cell exhaustion is a critical factor in the context of chronic viral infections. During persistent infections, T cells can enter a state of dysfunction characterized by reduced proliferation and effector function, which is often driven by sustained antigen exposure. This exhaustion can lead to an impaired ability to control viral replication [38]. Mechanistically, T cell exhaustion is associated with metabolic dysfunction, where the altered metabolic pathways in T cells limit their effectiveness in combating chronic infections [38].

Moreover, some viruses employ strategies that promote T cell exhaustion through the upregulation of inhibitory receptors on T cells, such as PD-1, which further dampens T cell responses. This strategy is particularly relevant in the context of HIV and hepatitis viruses, where the virus exploits the immune system's regulatory pathways to evade effective T cell-mediated responses [39].

Lastly, viral recombination is another mechanism through which T cells may be evaded. In HIV-1 infections, recombination between different viral strains can lead to the emergence of variants that escape T cell recognition, further complicating the host's ability to mount an effective immune response [36].

In summary, the mechanisms of T cell evasion by viruses are multifaceted, involving mutations in viral epitopes, manipulation of antigen presentation pathways, induction of T cell exhaustion, and the use of recombination to generate escape variants. Understanding these mechanisms is crucial for developing effective therapeutic strategies to enhance T cell responses against viral infections.

4.2 B Cell Response Modulation ​

Viral immune evasion is a critical aspect of viral pathogenesis, particularly concerning how viruses circumvent host immune responses to establish persistent infections. A significant area of focus is the modulation of B cell responses, which is essential for the production of antibodies that can neutralize viral pathogens.

Viruses employ several mechanisms to interfere with B cell responses. One prominent strategy is the alteration of the host cytokine milieu, which can influence B cell activation and differentiation. By modulating cytokine levels, viruses can promote the development of immunoregulatory cells that suppress effective B cell responses, thereby allowing the virus to persist in the host [40].

Moreover, viruses can induce the production of non-neutralizing antibodies that interfere with the activity of neutralizing antibodies (nAbs). This phenomenon, referred to as "neutralization interfering antibodies," can diminish the efficacy of the immune response, facilitating viral escape from neutralization [41]. Such mechanisms are particularly problematic in chronic infections, where robust humoral responses do not translate into effective viral clearance [41].

Additionally, viruses can exploit mechanisms related to the modulation of B cell immunodominance. This is the phenomenon where the immune response is skewed towards certain antigenic determinants, potentially neglecting others that may be critical for effective viral neutralization. By altering the expression of viral antigens or presenting them in a manner that shifts the focus of the immune response, viruses can evade recognition by B cells [42].

In the context of hepatitis C virus (HCV), studies have identified specific mutations that allow the virus to evade neutralizing antibodies by altering the use of host-cell entry factors. These mutations can affect virus-antibody interactions, leading to persistent infection [43]. This highlights the dynamic interplay between viral evolution and host immune responses, emphasizing the need for continuous adaptation by both the virus and the immune system.

Understanding these mechanisms is crucial for developing novel antiviral therapies and vaccines. By elucidating how viruses modulate B cell responses, researchers can design strategies that enhance the effectiveness of the immune response against viral infections, potentially leading to improved outcomes in managing chronic viral diseases [44].

5 Case Studies of Viral Immune Evasion ​

5.1 HIV ​

Human Immunodeficiency Virus (HIV) employs a multitude of sophisticated mechanisms to evade the host immune system, significantly complicating efforts to develop effective vaccines and therapeutic strategies. These mechanisms can be categorized into various strategies that target both the innate and adaptive immune responses.

  1. Genomic Mutations and Antigenic Variation: HIV is characterized by a high mutation rate, which allows it to rapidly alter its surface proteins. This is particularly evident in the envelope glycoprotein (Env), which is the primary target for neutralizing antibodies. HIV utilizes conformational changes in Env to present different antigenic states to the immune system, effectively hiding vulnerable epitopes from recognition. For instance, studies have shown that the Env glycoprotein can adopt conformations that are less recognizable to the immune system, thus allowing the virus to persist in the presence of robust antibody responses [45].

  2. Downregulation of Major Histocompatibility Complex (MHC) Molecules: HIV has developed mechanisms to downregulate MHC class I molecules on the surface of infected cells. This is achieved through viral proteins such as Nef, which mediates the internalization of MHC-I molecules from the cell surface, thereby reducing the visibility of infected cells to CD8+ T cells [46]. Additionally, the Tat protein can repress MHC-I transcription, further impairing the ability of the immune system to recognize and eliminate infected cells [46].

  3. Formation of Latent Viral Reservoirs: HIV can establish latent reservoirs in the host, where the virus remains dormant within infected cells, evading immune detection. These reservoirs can reactivate under certain conditions, leading to renewed viral replication and disease progression [47].

  4. Interference with Innate Immune Responses: HIV exploits various host factors to evade detection by the innate immune system. For example, it can suppress the activity of restriction factors such as APOBEC3G and TRIM5α, which are part of the intrinsic immune defense against viral infections [48]. Furthermore, HIV can manipulate host proteins involved in DNA sensing, such as TREX1, to evade recognition by the immune system [28].

  5. Exploitation of Immune Cell Mechanisms: HIV can induce apoptosis in immune cells, particularly CD4+ T cells, thereby depleting a critical component of the adaptive immune response. This strategy not only reduces the number of immune cells available to combat the infection but also contributes to a state of chronic immune activation, which can lead to immune exhaustion [23].

  6. Natural Killer (NK) Cell Evasion: HIV can escape NK cell-mediated immune pressure by mutating specific epitopes presented by MHC class I molecules. For instance, certain mutations in the p24 Gag protein were found to enhance binding to inhibitory receptors on NK cells, thereby diminishing the activation of these immune cells against HIV-infected targets [49].

  7. Induction of Immune Dysfunction: HIV infection leads to a broad dysfunction of the immune system, including clonal expansion and excessive activation of T cells, resulting in immunosenescence and exhaustion [50]. This dysfunction impairs the overall ability of the immune system to mount effective responses against the virus.

Understanding these mechanisms of immune evasion is crucial for the development of novel therapeutic and vaccine strategies aimed at overcoming the challenges posed by HIV. Insights into how HIV manipulates the immune response can guide researchers in designing interventions that enhance immune recognition and clearance of the virus.

5.2 Influenza Virus ​

Influenza viruses exhibit a variety of mechanisms to evade host immune responses, which is critical for their survival and replication. These mechanisms involve both the direct manipulation of host cellular processes and the alteration of immune signaling pathways.

One prominent mechanism of immune evasion by the influenza virus is the function of the non-structural protein 1 (NS1). NS1 inhibits type I interferon (IFN) signaling pathways, which are essential for antiviral responses. In a study, it was shown that mice infected with an NS1-expressing influenza A H1N1 virus exhibited lower expression levels of IFNβ in the lungs. Additionally, human alveolar epithelial A549 cells infected with the H1N1 virus produced antiviral IFNβ, but transfection with H1N1 NS1 resulted in the loss of this ability, indicating that NS1 interferes with both the production of IFNβ and the expression of IFN receptors. Furthermore, NS1 inhibits the activation of signal transducers and activators of transcription (STAT)1 and STAT2, which are crucial for the downstream signaling of IFNβ production, thus playing a significant role in the virus's evasion strategy [51].

Another mechanism involves host shutoff, where the influenza virus down-regulates host gene expression to take control of the infected cells. This process is facilitated by several viral proteins, including NS1, the RNA-dependent RNA polymerase, and the endoribonuclease PA-X. These proteins contribute to the alteration of translation, RNA synthesis, and stability, thereby hindering the host's immune response and facilitating viral replication [52].

Additionally, influenza viruses employ strategies to evade natural killer (NK) cell recognition. The neuraminidase (NA) protein plays a crucial role in this process by removing sialic acid residues from the NKp46 receptor on NK cells, which diminishes the recognition of hemagglutinin (HA) on infected cells. This mechanism highlights how the virus can interfere with innate immune responses, particularly those mediated by NK cells, thereby enhancing its survival [53].

The virus also activates various pathways that suppress host innate immunity. For instance, the epidermal growth factor receptor (EGFR) and extracellular signal-regulated kinase (ERK) signaling pathways are activated upon influenza A virus infection, leading to the suppression of type I and III IFNs and interferon-stimulated genes (ISGs). This activation of EGFR/ERK signaling is facilitated by the protein tyrosine phosphatase SHP2, which plays a critical role in modulating antiviral responses [54].

Moreover, influenza viruses can induce host shut-off mechanisms that disrupt the production of type I IFNs. The viruses exploit various host proteins involved in the IFN signaling pathway, such as tripartite motif containing 25 (TRIM25) and mitochondrial antiviral signaling protein (MAVS), to evade detection and inhibit effective immune responses [55].

In summary, influenza viruses utilize multiple strategies to evade host immune responses, including the inhibition of IFN signaling through NS1, host shutoff mechanisms, alteration of NK cell recognition via neuraminidase, and the activation of signaling pathways that suppress antiviral responses. These mechanisms collectively enhance the virus's ability to replicate and persist within the host.

5.3 SARS-CoV-2 ​

SARS-CoV-2 employs multiple sophisticated mechanisms to evade the host's immune system, which are critical for its pathogenesis and the persistence of infection. The following outlines key strategies identified in recent studies.

One primary mechanism is the suppression of type I interferon (IFN) production, which is crucial for initiating the innate immune response. SARS-CoV-2 achieves this through various non-structural proteins (NSPs) and accessory proteins that interfere with the signaling pathways involved in IFN production. For instance, NSP2 has been shown to repress the translation of IFN-β mRNA by interacting with the cellular protein GIGYF2, which enhances the binding of GIGYF2 to the mRNA cap-binding protein 4EHP, leading to reduced IFN-β synthesis [56]. Additionally, the virus can downregulate the expression of major histocompatibility complex class I (MHC-I) molecules through proteins such as ORF6 and ORF8, thus hindering the recognition of infected cells by cytotoxic T lymphocytes [2].

SARS-CoV-2 also targets the innate immune cells directly. It can exhaust natural killer (NK) cell-mediated cytotoxicity by downregulating stress ligands recognized by the NKG2D receptor on NK cells [57]. Furthermore, the virus can impair the activation of pattern recognition receptors (PRRs) that are essential for the detection of viral components, thereby compromising the signaling pathways that lead to the activation of immune responses [58].

Another significant mechanism of immune evasion involves the induction of a hyper-inflammatory response, known as a cytokine storm, which can lead to severe tissue damage and further complications in COVID-19 patients. SARS-CoV-2 triggers the overactivation of the NLRP3 inflammasome, resulting in the excessive release of pro-inflammatory cytokines [59]. This dysregulation of the immune response not only allows the virus to persist but also contributes to the pathogenesis of severe disease [60].

The virus's ability to generate extracellular vesicles (EVs) has also been implicated in immune evasion. These EVs can facilitate cell-to-cell transmission of the virus while evading neutralizing antibodies, thereby promoting viral spread without triggering an effective immune response [61].

Additionally, SARS-CoV-2 can exploit host cellular pathways to its advantage. For example, it can hijack cellular machinery involved in protein synthesis and metabolism to favor its replication while simultaneously inhibiting the host's antiviral responses [62].

Overall, the intricate mechanisms of immune evasion employed by SARS-CoV-2 highlight the challenges in developing effective therapeutic strategies and vaccines against this virus. Understanding these mechanisms is crucial for advancing antiviral therapies and improving pandemic preparedness [63][64].

6 Implications for Vaccine Development ​

7 Conclusion ​

The mechanisms of viral immune evasion are intricate and multifaceted, significantly complicating our understanding of viral pathogenesis and the development of effective therapeutic strategies. This review highlights key strategies employed by various viruses, including the alteration of viral antigens, inhibition of interferon signaling, disruption of antigen presentation, and modulation of apoptotic pathways. Notably, viruses like HIV, Influenza, and SARS-CoV-2 exemplify how these evasion tactics can undermine both innate and adaptive immune responses. The continuous evolution of viral strains further exacerbates the challenge of vaccine development, necessitating ongoing research to elucidate these mechanisms. Future studies should focus on identifying novel therapeutic targets that can enhance immune recognition and clearance of viral infections. Moreover, integrating insights from viral immune evasion mechanisms into vaccine design could pave the way for more effective interventions against persistent viral diseases, ultimately improving public health outcomes.

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